Striatal and Cortical β-Amyloidopathy and Cognition in Parkinson's Disease

Neha Shah, Kirk A. Frey, Martijn L.T.M Müller, Myria Petrou, Vikas Kotagal, Robert A. Koeppe, Peter J.H. Scott, Roger L. Albin, Nicolaas I. Bohnen

Research output: Contribution to journalArticle

Abstract

Introduction: Although most previous cognitive studies of β-amyloidopathy in PD focused on cortical plaque deposition, recent postmortem studies point to an important role of striatal β-amyloid plaque deposition. The aim of this study was to investigate the relative contributions of striatal and cortical β-amyloidopathy to cognitive impairment in PD. Methods: Patients with PD (n = 62; age, 68.9 ± 6.4 years; H & Y stage: 2.7 ± 0.5; MoCA score: 25.2 ± 3.0) underwent [11C]Pittsburgh compound B β-amyloid, [11C]dihydrotetrabenazine monoaminergic, and [11C]methyl-4-piperidinyl propionate acetylcholinesterase brain PET imaging and neuropsychological assessment. [11C]Pittsburgh compound B β-amyloid data from young to middle-aged healthy subjects were used to define elevated [11C]Pittsburgh compound B binding in patients. Results: Elevated cortical and striatal β-amyloid deposition were present in 37% and 16%, respectively, of this predominantly nondemented cohort of patients with PD. Increased striatal β-amyloid deposition occurred in half of all subjects with increased cortical β-amyloid deposition. In contrast, increased striatal β-amyloid deposition did not occur in the absence of increased cortical β-amyloid deposition. Analysis of covariance using global composite cognitive z scores as the outcome parameter showed significant regressor effects for combined striatal and cortical β-amyloidopathy (F = 4.18; P = 0.02) after adjusting for covariate effects of cortical cholinergic activity (F = 5.67; P = 0.02), caudate nucleus monoaminergic binding, duration of disease, and age (total model: F = 3.55; P = 0.0048). Post-hoc analysis showed significantly lower cognitive z score for combined striatal and cortical β-amyloidopathy, compared to cortical-only β-amyloidopathy and non-β-amyloidopathy subgroups. Conclusions: The combined presence of striatal and cortical β-amyloidopathy is associated with greater cognitive impairment than cortical β-amyloidopathy alone in PD.

Original languageEnglish (US)
Pages (from-to)111-117
Number of pages7
JournalMovement Disorders
Volume31
Issue number1
DOIs
StatePublished - Jan 1 2016

Keywords

  • Acetylcholinesterase
  • Cognitive impairment
  • Cortex
  • Dopamine
  • PET
  • Parkinson's disease
  • Striatum
  • β-amyloid

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

Fingerprint Dive into the research topics of 'Striatal and Cortical β-Amyloidopathy and Cognition in Parkinson's Disease'. Together they form a unique fingerprint.

  • Cite this

    Shah, N., Frey, K. A., L.T.M Müller, M., Petrou, M., Kotagal, V., Koeppe, R. A., Scott, P. J. H., Albin, R. L., & Bohnen, N. I. (2016). Striatal and Cortical β-Amyloidopathy and Cognition in Parkinson's Disease. Movement Disorders, 31(1), 111-117. https://doi.org/10.1002/mds.26369